The brain derives most of its energy from the oxidative metabolism of glucose. Since there is good evidence correlating the utilization of the energy source - glucose - with neuronal activity, there is reason to expect that altered CNS activity might be reflected by regional changes in levels of the oxidative enzymes as well. The P.I. has shown that chronic disuse or electrical stimulation results in marked reduction or increase, respectively, of the level of an oxidative enzyme, cytochrome oxidase, in appropriate parts of the nervous system. Such enzymatic alterations occur not only when the experimental manipulations are done in the neonate or during the critical period, but also in the adult when the nervous system is throught to be refractory to sensory deprivation. Whisker removal in the adult mice has resulted in a dramatic decrease of C.O. activity in the cortical barrels, despite "normal" cytoarchitecture. We now proposed to examine the barrels at the E.M. level to determine if the change is related to a decrease in the number of mitochondria, or a decrease in the relative level of C.O. activity per mitochondrion, or a combination of the above in different neuronal profiles. We will also perform lid sutures on adult cats to determine if the appropriate geniculate laminae will be affected. If so, we wish to localize the decrease in C.O. activity to specific neuronal elements of known origin, such as primary afferent terminals, postsynaptic dendrites, presynaptic dendrites, or other terminals such as cortical feedback fibers. Finally, we wish to know to what extent are these enzymatic alterations impulse dependent. We will introduce tetrodotoxin intravitreally to block afferent impulses to the geniculate, without blocking axoplasmic transport. The LGN will be examined at the light microscopic level for any changes in the level of C.O. activity. These data will help us to gain better understanding of the correlation between functional demand and enzymatic adjustment, as well as the degree of susceptability of adult nervous system to varying forms of sensory deprivation.